Pathology of choroid plexus in spontaneous immune complex disease and chronic viral infections.

Abstract

Using immunofluorescence and electron microscopy, deposits of immunoglobulin G (IgG) and the third complement component (C3) are found in the choroid plexus of mice with spontaneous immune complex disease, in mice chronically infected with lymphocytic choriomeningitis (LCM) virus and in patients with systemic lupus erythematosus (SLE). (NZB × W) F1 mice develop antibodies to nuclear antigen (ANA) and DNA (ADNA) and are an animal model of human SLE. Enhancement of ANA and ADNA responses by immunization with DNA leads to accelerated and more severe involvement of the choroid plexus accompanied by leukocytic infiltrates. Mice infected in utero or at birth with LCM virus harbor the virus throughout life and continuously produce antibodies. Virus and antiviral antibody(s) combine in the serum and form immune complexes that are trapped in renal glomeruli and choroid plexus. In contrast, mice chronically infected with scrapie fail to show immunoglobulin deposits in choroid plexus and brain despite clinical and pathological evidence of severe scrapie encephalopathy. The findings indicate that the choroid plexus is a favored site for the trapping of immune complexes and may be damaged during immune complex disease. Choroid plexus injury could lead to spinal fluid changes that may be responsible in part for neurologic and psychiatric disturbances seen in patients with systemic lupus erythematosus, chronic and acute viral infections and other disorders associated with circulating antigen-antibody complexes.